Institute of Parasitology, Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Längggassstrasse 122, 3012, Bern, Switzerland.
Institute of Parasitology, Department of Infectious Diseases and Pathobiology, Vetsuisse Faculty, University of Bern, Längggassstrasse 122, 3012, Bern, Switzerland.
Int J Parasitol Drugs Drug Resist. 2020 Aug;13:121-129. doi: 10.1016/j.ijpddr.2020.06.002. Epub 2020 Jul 2.
The current chemotherapeutical treatment against alveolar echinococcosis relies exclusively on benzimidazoles, which are not parasiticidal and can induce severe toxicity. There are no alternative treatment options. To identify novel drugs with activity against Echinococcus multilocularis metacestodes, researchers have studied potentially interesting drug targets (e.g. the parasite's energy metabolism), and/or adopted drug repurposing approaches by undertaking whole organism screenings. We here focus on drug screening approaches, which utilize an in vitro screening cascade that includes assessment of the drug-induced physical damage of metacestodes, the impact on metacestode viability and the viability of isolated parasite stem cells, structure-activity relationship (SAR) analysis of compound derivatives, and the mode of action. Finally, once in vitro data are indicative for a therapeutic window, the efficacy of selected compounds is assessed in experimentally infected mice. Using this screening cascade, we found that the anti-malarial mefloquine was active against E. multilocularis metacestodes in vitro and in vivo. To shed more light into the mode of action of mefloquine, SAR analysis on mefloquine analogues was performed. E. multilocularis ferritin was identified as a mefloquine-binding protein, but its precise role as a drug target remains to be elucidated. In mice that were infected either intraperitoneally with metacestodes or orally with eggs, oral treatment with mefloquine led to a significant reduction of parasite growth compared to the standard treatment with albendazole. However, mefloquine was not acting parasiticidally. Assessment of mefloquine plasma concentrations in treated mice showed that levels were reached which are close to serum concentrations that are achieved in humans during long-term malaria prophylaxis. Mefloquine might be applied in human AE patients as a salvage treatment. Future studies should focus on other repurposed anti-infective compounds (MMV665807, niclosamide, atovaquone), which showed stronger in vitro activity against E. multilocularis than mefloquine.
当前针对泡型包虫病的化学治疗方法完全依赖苯并咪唑类药物,但这些药物没有杀虫作用,而且可能会引起严重的毒性。目前尚无其他治疗选择。为了寻找具有抗细粒棘球蚴活性的新药,研究人员已经研究了潜在的有意义的药物靶点(例如寄生虫的能量代谢),并通过进行全生物体筛选采用了药物再利用方法。我们在此重点介绍药物筛选方法,该方法利用体外筛选级联,包括评估药物对包虫蚴的物理损伤、对包虫蚴活力和分离的寄生虫干细胞活力的影响、化合物衍生物的结构-活性关系(SAR)分析以及作用方式。最后,一旦体外数据表明存在治疗窗口,就会在实验感染的小鼠中评估选定化合物的疗效。使用该筛选级联,我们发现抗疟药甲氟喹对体外和体内的细粒棘球蚴包虫蚴均具有活性。为了进一步阐明甲氟喹的作用方式,对甲氟喹类似物进行了 SAR 分析。细粒棘球蚴铁蛋白被鉴定为甲氟喹结合蛋白,但它作为药物靶点的确切作用仍有待阐明。在经腹腔接种包虫蚴或口服虫卵感染的小鼠中,与阿苯达唑标准治疗相比,口服甲氟喹治疗可显著减少寄生虫的生长。但是,甲氟喹并没有杀虫作用。对接受治疗的小鼠中甲氟喹的血浆浓度评估表明,达到了在人类进行长期疟疾预防时达到的接近血清浓度的水平。甲氟喹可能被用作人类泡型包虫病患者的挽救治疗。未来的研究应集中在其他重新利用的抗感染化合物(MMV665807、硝氯酚、阿托伐醌)上,这些化合物对细粒棘球蚴的体外活性强于甲氟喹。